Ординатура / Офтальмология / Английские материалы / Rapid Diagnosis in Ophthalmology Series Anterior Segment_Macsai, Machado Fontes_2007

Cornea • 5 SECTION

Fungal Keratitis

Key Facts

•Important cause of visual loss in developing countries

•Incidence, risk factors, and causative agent vary among different geographic regions

•Two classic basic forms described:

1.Caused by filamentous fungi (especially Fusarium and Aspergillus )

•Trauma is the key predisposing factor, more common in healthy young males

2.Caused by yeast-like and related fungi (particularly Candida)

•Usually concomitant pre-existing ocular and/or systemic disease

Clinical Findings

•Firm elevated areas, hyphate lines extending into unaffected cornea

•Multifocal granular (or feathery) grey-white satellite stromal infiltrates

•Immune ring or nummular midstromal infiltrates

•Descemet’s folds, iritis, endothelial plaque, hypopyon

Ancillary Testing

•Microbiologic investigation (material obtained by corneal scraping or biopsy)

•Microscopy: potassium hydroxide 10%, gram, Giemsa, periodic acid Schiff, calcofluor white

•Culture (may require incubation for ≤4–6 weeks): blood agar, brain–heart infusion agar, Sabouraud agar, thioglycolate broth

Differential Diagnosis

•Bacterial keratitis

•Herpetic keratitis

Treatment

•First-line therapy for superficial keratitis (continued for ≥6 weeks):

•topical natamycin 5% or amphotericin B 0.15% (hourly around the clock for several days)

•deep lesions necessitate subconjunctival and/or systemic therapy as well (miconazole, ketoconazole, itraconazole, fluconazole)

•Surgical treatment includes:

•debridement of infected or necrotic tissue • conjunctival flaps • tissue adhesives • penetrating keratoplasty

•Cycloplegics

Prognosis

•Can lead to blindness in a few weeks depending on interplay of agent, host, and predisposing factors

•Slow response to treatment can be expected, corticosteroids can lead to worsening

•15–27% of patients require surgical intervention because of failure of medical therapy

Fig. 5.127 Aspergillus keratitis: severe ocular infl ammation, corneal immune ring, and hypopyon.

Fig. 5.128 Grey-white elevated corneal lesion with undistinct margins and satellite infiltrates.

Keratitis Fungal

Fig. 5.129 Fusarium solani keratitis: extensive lesion with associated hypopion. (Courtesy of the External Eye Disease and Cornea Section, Federal University of Sao Paulo, Brazil.)

Fig. 5.130 Candida keratitis in a diabetic patient. (Courtesy of the External Eye Disease and Cornea Section, Federal University of Sao Paulo, Brazil.)

Fig. 5.131 Perforated Aspergillus keratitis. Shallow anterior chamber and hypopion.

Fig. 5.132 Fusarium keratitis: indistinct feathered edges and diffuse stromal invasion. (Courtesy of the External Eye

Disease and Cornea Section, Federal 161 University of Sao Paulo, Brazil.)

Cornea • 5 SECTION

Atypical Bacteria

Key Facts

•Opportunistic pathogens—requires alteration in normal environment to cause infection

•Non-tuberculous or atypical mycobacteria are the most common etiologic factors in post-LASIK infections

•Clusters or outbreaks in laser vision correction centers around the world have been described

•Mycobacterium species found in:

• water • milk • soil • animals • scrub sinks • skin • sputum • the environment

•Rod-shaped, non-motile, non–spore-forming aerobic bacteria referred to as acidfast bacilli

•Indolent course, with delayed onset of symptoms (usually 1–3 weeks) after risk event (e.g. trauma or surgery)

Clinical Findings

•Focal, round, or dot-like whitish infiltrates • Dust-like ring of tiny white opacities surrounding a major larger infiltrate • Cracked windshield appearance

• Satellite lesions • Flap necrosis (if after LASIK)

Ancillary Testing

•Microbiologic evaluation (corneal scraping or biopsy):

•smears (gram, Giemsa, Ziehl–Neelsen, fluorochrome stains)

•culture (blood and chocolate agar, thioglycolate broth, Lowenstein–Jensen media)

•antimicrobial susceptibility testing

•PCR

Differential Diagnosis

•Bacterial (especially Nocardia and Corynebacterium) or fungal

keratitis • Infectious crystalline keratopathy • Diffuse lamellar keratitis

Treatment

•Topical antibiotics:

•tobramycin 14 mg/mL • amikacin 50 mg/mL • clarithromycin 10 mg/mL • ofloxacin 3 mg/mL • azithromycin 2 mg/mL • fluoroquinolones (gatifloxacin 0.3% or moxifloxacin 0.5%)

•Systemic clarithromycin (500 mg twice a day)

•Surgical debridement or therapeutic lamellar keratectomy (sometimes flap removal is necessary)

•Topical cycloplegics

•Steroids are contraindicated

Prognosis

•Location in the flap interface after LASIK can make it more difficult to obtain samples for microbiologic evaluation and prevent adequate concentration of antibiotics

•Sight-threatening infection

•Early diagnosis and institution of appropriate treatment are crucial to satisfactory outcome

•Long-term treatment—patient compliance is crucial

Fig. 5.134 Mycobacteria keratitis (acute phase): cornel infi ltrates with multiple dots and crystalline keratopathy. (Courtesy of Filipe A. Gusmao, MD.)

Fig. 5.136 Mycobacteria keratitis: healing phase. (Courtesy of Filipe A. Gusmao, MD.)

Fig. 5.133 Corneal biopsy showing the mycobacterium. (Courtesy of Filipe A. Gusmao, MD.)

Bacteria Atypical

Fig. 5.135 Irregular infi ltrate, indistinct margins, and satellite lesions. (Courtesy of Filipe A. Gusmao, MD.)

Fig. 5.137 Mycobacteria keratitis: healing phase. (Courtesy of Filipe A. Gusmao, MD.)

Cornea • 5 SECTION

Acanthamoeba Keratitis

Key Facts

•Contact lens wear is strongest risk factor, with soft hydrogel lenses responsible for most cases

•Incidence of one case per 30 000 contact lens wearers per year

•Acanthamoeba can be isolated from about 15% of contact lens storage cases and is also found in:

• chlorinated swimming pools • showers • jacuzzis • fountains • sandy beaches

• seawater • ocean sediment • sewage outfalls

•Use of tap water for contact lens hygiene is strongly related to infection (source of Acanthamoeba)

•Only four Acanthamoeba genotypes (T3, T4, T6, and T11) have been associated with keratitis

•The organism is characterized by a life cycle of feeding and replicating trophozoite and dormant cyst stages

•Characteristic symptom is a disproportionately severe ocular pain not commensurate with clinical findings

Clinical Findings

•Paracentral ring-like stromal infiltrate, epithelial haze • Epithelial defects and stromal nummular infiltrates • Dendritiform ulcers, epithelial irregularities and erosions • Limbitis or radial keratoneuritis • Diffuse or nodular scleritis, anterior chamber reaction

Ancillary Testing

•Corneal scrapings and biopsy to microbiologic evaluation

•direct microscopy (calcofluor white, gram, Giemsa, acridine orange)

•culture (Escherichia coli plated on non-nutrient agar 1.5%)

•Confocal microscopy or PCR

Differential Diagnosis

• Herpetic keratitis • Bacterial or fungal keratitis

Treatment

•Epithelial debridement improves penetration of drugs into cornea and should be done in early phases • Propamidine isethionate 0.1% (Brolene) • Polyhexamet hylene biguanide 0.02% • Topical chlorhexidine 0.02% • Neomycin–polymyxin B–gramicidin • Systemic ketoconazole (200–600 mg/day) • Penetrating keratoplasty when impending perforation • Topical cycloplegics and nonsteroidal anti-inflammatory drugs • Steroids have a deleterious effect and are contraindicated

Prognosis

•Vision-threatening disease—permanent visual loss in >30% of patients and enucleation in recalcitrant cases

•The resistance of Acanthamoeba cysts to most antimicrobial agents makes it one of the most difficult ocular infections to treat, with a mean treatment period of >5 months and surgical interventions in ≤50% of cases

•Patient’s compliance to treatment is difficult but critical

•Graft recurrence of the infection is common, so penetrant keratoplasty should be delayed until the disease is under control

Fig. 5.138 Acanthamoeba infection in a soft contact lens wearer. Nummular lesions with little conjunctival injection.

Fig. 5.140 Typical sign: radial neuritis. A pain disproportional to the extent of corneal inflammation is usually found in these patients.

Fig. 5.142 Another example of evident corneal nerve infl ammation in acanthamoebic keratitis. (Courtesy of Denise de Freitas, MD.)

Fig. 5.139 Same patient as in Fig. 5.138: fl uorescein staining due to epithelial defect.

Fig. 5.141 Dendritiform epithelial lesions. Herpetic keratitis is one differential diagnosis. (Courtesy of Denise de Freitas, MD.)

Fig. 5.143 Immune ring in amoebic keratitis, with surrounding edema. Pronounced ciliary injection. (Courtesy of Denise de Freitas, MD.)

Keratitis Acanthamoeba

Cornea • 5 SECTION

Corneal Abrasion

Key Facts

•One of the most common eye injuries, with an estimated incidence of 789 in 100 000

•Most commonly seen after a tangential impact from a foreign body, radiation, heat and chemical trauma

•Keep in mind that occult ocular injuries may be present

Clinical Findings

•Topical anesthetic facilitates the examination, which shows:

• conjunctival hyperemia

•loss of corneal luster

•epithelial defect with surrounding loose epithelium

•a granular anterior stromal infiltrate underlying the defect (if the examination is delayed)

•normal anterior chamber

Ancillary Testing

• Clinical diagnosis (history and slit-lamp examination with fluorescein staining)

Differential Diagnosis

•Factitious keratoconjunctivitis

•Source of injury (mechanical, chemical, thermal)

Treatment

• Topical cycloplegic

•Topical broad-spectrum antibiotic (e.g. fluoroquinolone or aminoglycoside)

•Bandage contact lens (preferable), taping of lids, or application of a pressure patch

Prognosis

•Most cases have a favorable outcome, with complete healing in 1–2 days

•Bowman’s membrane lesion leads to scarring

•Increased risk for bacterial infection while epithelial defect exists—close followup is warranted

Fig. 5.144 Traumatic corneal lesion (piece of paper). This patient had epithelial erosion 2 weeks after total wound healing.

Cornea • 5 SECTION

Recurrent Erosion Secondary to Trauma

Key Facts

•Can be secondary to trivial trauma (e.g. from a fingernail, the edge of paper, or a leaf of a tree)

•Characterized by repeated episodes of pain, photophobia, watering, redness, and tearing, especially on awakening

•Related to poor adhesion of corneal epithelium to underlying stroma

•Incidence is about 1 in 150 cases following traumatic corneal abrasion

Clinical Findings

•Most commonly occurring within lower half of cornea

•Corneal epithelial defects

•Loosely adherent and elevated epithelium

•Epithelial microcysts

•Stromal infiltrates and/or opacities

Ancillary Testing

• Clinical diagnosis (history and slit-lamp examination)

Differential Diagnosis

•Factitious keratoconjunctivitis

•Exposure keratitis or neurotrophic keratopathy

•Herpetic keratitis

•Foreign bodies under tarsal plate

Treatment

•Clinical:

•patching, cycloplegia, topical lubrication and antibiotics, bandage contact lens

•autologous serum, oral doxycycline, botulinum toxin–induced ptosis

•Surgical:

•diamond burr polishing of Bowman’s membrane

•anterior stromal puncture

•phototherapeutic keratectomy

Prognosis

•May rarely lead to visual disability

•Most cases respond well to conservative (clinical) treatment

•Corneal infiltrates and infectious keratitis may develop at site of corneal erosions

•Long-term use of contact lenses may predispose to bacterial keratitis, vascularization, and scarring

Cornea • 5 SECTION

Factitious Keratoconjunctivitis

Key Facts

•Psychopathologic condition in which symptoms or physical findings are intentionally produced in order to assume the sick role

• Self-induced or accidental trauma is emphatically denied

•Rare and difficult to diagnose condition

•Can result from mechanical or chemical trauma

•Most common in military personnel and medical field employees

•A confession as to self-inflicting an artificial ocular disease is attained in only few patients

Clinical Findings

•Chronic (usually >3 weeks) conjunctivitis with peculiar characteristics:

•purulent discharge • nearly always localized inferiorly (with quiet superior bulbar conjunctiva) • severe hyperemia and mild chemosis • punctate keratopathy, coarse focal keratopathy, persistent epithelial defect

•Filamentary keratopathy or pseudodendrites

Ancillary Testing

• Clinical diagnosis (history and slit-lamp examination)

Differential Diagnosis

•Toxic keratoconjunctivitis, allergic diseases, blepharitis, dry eye

•Munchausen syndrome by proxy, malingering, neurologic disorders

•Mucus fishing syndrome, congenital or acquired corneal anesthesia

•Topical anesthetic abuse

Treatment

•Depends on extent and presentation of each case:

•patching, bandage contact lens, topical antibiotics, and preservative-free artificial tears

•Sometimes requires hospitalization

•Psychiatric evaluation is typically indicated

Prognosis

•Visual outcome depends on extent of self-inflicted damage

•Dramatic improvement of clinical findings is found when patient is placed under 24-h observation